Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Among patients with rheumatoid arthritis (RA), traditional risk factors for cardiovascular disease (CVD) mostly predicted atherosclerotic CVD (ASCVD), except for obesity, which was a risk factor for unprovoked venous thromboembolism (VTE).

Major finding: Obesity was associated with increased VTE risk (adjusted hazard ratio [aHR], 1.47; 95% confidence interval [CI], 1.14-1.89) and reduced ASCVD risk (aHR, 0.56; 95% CI, 0.48-0.66). Other traditional CVD risk factors such as diabetes (aHR, 1.39; 95% CI, 1.20-1.62), hypertension (aHR, 1.21; 95% CI, 1.07-1.39), and chronic kidney disease (aHR, 1.31; 95% CI, 1.10-1.66) predicted higher ASCVD risk.

Study details: The data come from an analysis of 31,366 patients with RA from a US-wide longitudinal observational registry, who did not have any prior CVD at baseline and active cancer throughout follow-up.

Disclosures: No sources of funding were reported. K Michaud reported receiving grant support from the Rheumatology Research Foundation. No competing interests were declared.

Source: Ozen G et al. RMD Open. 2021 Jun 30. doi: 10.1136/rmdopen-2021-001618.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Patients with rheumatoid arthritis (RA) receiving interleukin-6 inhibition (IL-6i) therapy with or without T-cell inhibitors had a significantly lower risk for type 2 diabetes mellitus (T2DM) vs those receiving tumor necrosis factor inhibitors (TNFi) or not receiving any biological disease-modifying antirheumatic drugs (bDMARDs).

Major finding: Compared with patients not receiving bDMARDs, those who received IL-6i and IL-6i+T-cell inhibitors had a significant 37% (hazard ratio [HR], 0.63; P = .021) and 34% (HR, 0.66; P = .019) lower risk for T2DM, respectively, whereas no significant difference was observed among patients receiving TNFi (HR, 0.99; P = .26) and T-cell inhibitors (HR, 0.96; P = .37).

Study details: This was a retrospective cohort study of 283,756 patients with RA categorized as bDMARD recipients (TNFi, n=34,873; IL-6i, n=1,884; T-cell inhibitors, n=5,935; and IL-6i+T-cell inhibitor abatacept, n=1,213) and non-bDMARD recipients (n=125,337).

Disclosures: This study was supported by Roche/Genentech. The principal author reported receiving grants, consultancy, and/or speaker fees from various sources. JH Best, S Gale, and K Sarsour reported being employees of Genentech.

Source: Paul SK et al. BMJ Open. 2021 Jun 16. doi: 10.1136/bmjopen-2020-042246.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Despite limited radiological damage, rapid radiological progression (RRP) still occurred in about 1 of 5 patients in a real-world cohort of patients with rheumatoid arthritis (RA) treated to the target of remission. RRP was most strongly predicted by baseline erosive disease.

Major finding: Most radiological damage occurred in the first year of treatment vs subsequent 5 years of follow-up (median Sharp/van der Heijde score, 2.0 vs 3.0). Despite achieving low disease activity, almost 18.8% of the patients developed RRP within 6 months, and the number of patients with erosive disease increased from 16% at baseline to 58% at 6 years. The erosive disease was the strongest predictor of RRP (odds ratio, 8.8; P less than .001).

Study details: Findings are from the observational DREAM remission induction cohort involving 219 patients diagnosed with RA who had at least 1 radiograph of hands and feet at baseline and at least 1 additional pair of radiographs during 6 years of follow-up and were treated to the target of remission.

Disclosures: No external funding and/or potential conflicts of interest were reported.

Source: Versteeg GA et al. Scand J Rheumatol. 2021 Jun 21. doi: 10.1080/03009742.2021.1917161.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Sarcopenia and low muscle mass are common comorbidities among middle-aged and elderly patients with rheumatoid arthritis (RA). Corticosteroid therapy was positively and conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) were inversely associated with sarcopenia.

Major finding: Overall, the prevalence of low muscle mass and sarcopenia was 30.2% (95% confidence interval [CI], 24.2%-36.2%). The use of csDMARDs was inversely (odds ratio [OR], 0.70; P = .019) and corticosteroid was positively (OR, 1.46; 95% CI, 0.94-2.29) associated with sarcopenia. No association was observed between biological/targeted DMARDs and sarcopenia (OR, 0.83; P = .420).

Study details: Findings are from a meta-analysis of 16 observational studies involving 2,240 middle-aged and older adults with RA.

Disclosures: No specific funding was received for this study. All the authors declared no conflicts of interest.

Source: Dao T et al. Calcif Tissue Int. 2021 Jun 16. doi: 10.1007/s00223-021-00873-w.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: Almost one-third of patients with new-onset rheumatoid arthritis (RA) had long-lasting unacceptable pain. Patients with a less inflammatory disease at baseline, in the form of lower swollen joint count (SJC), were at an increased risk for unacceptable pain at 5 years.

Major finding: Almost 49.1% of patients had unacceptable pain at inclusion, which decreased to 30.1% during the first year and remained unchanged thereafter. At 5 years, lower SJC (adjusted odds ratio [aOR] per standard deviation, 0.61; P = .01) was a significant predictor of unacceptable pain.

Study details: The data come from an inception cohort of 232 patients with early RA with symptom duration of at least 12 months.

Disclosures: This work was supported by the Swedish Research Council, the Swedish Rheumatism Association, and Lund University. Some of the authors declared receiving grants, personal fees, and lecture/consulting fees from and/or being an employee of or working as a medical advisor for various sources.

Source: Eberhard A et al. Arthritis Res Ther. 2021 Jun 14. doi: 10.1186/s13075-021-02550-7.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: The long-term safety profile of sarilumab was consistent with prior clinical studies and postmarketing reports in patients with rheumatoid arthritis (RA) refractory to tumor necrosis factor inhibitors (TNFi).

Major finding: Incidence rates of adverse events (AEs) and serious AEs were 160.4 and 10.2 per 100 patient-years (PY), respectively, with 132 discontinuations (8.1/100 PY). The rate of serious infections was 3.9 per 100 PY. Grade 3/4 neutropenia was observed in 14% of patients and normalized on treatment in 65% of patients. Clinical efficacy was sustained throughout the 5-year follow-up.

Study details: Findings are from the open-label extension (OLE), EXTEND study, which included 454 patients with TNFi-refractory RA who completed the phase 3 TARGET study. In the OLE, patients received sarilumab 200 mg twice per week plus conventional synthetic disease-modifying antirheumatic drugs.

Disclosures: This work was supported by Sanofi (Cambridge, MA, USA) and Regeneron Pharmaceuticals, Inc. (Tarrytown, NY, USA). Some of the authors reported receiving research grants and/or consulting fees from various sources. Some authors declared being an employee of and/or holding stocks/stock options at Sanofi or Regeneron Pharmaceuticals, Inc.

Source: Fleischmann R et al. Rheumatology (Oxford). 2021 Jun 24. doi: 10.1093/rheumatology/keab355.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.

Key clinical point: Systemic glucocorticoids (GCs) were effective at reducing pain in patients with active rheumatoid arthritis (RA), with the effect being greatest within 3 months of initiation, whereas it appeared to be less effective beyond 6 months.

Major finding: Treatment with systemic GCs significantly decreased spontaneous pain (standardized mean differences [MD], −0.67; 95% confidence interval [CI], −0.84 to −0.50), with the effect being greatest at 3 months or lesser (MD, −14.55 mm; 95% CI, −20.40 to −8.69) and appeared to be less effective at more than 3 to 6 months (MD, −7.82 mm; 95% CI, −12.27 to -3.38) and beyond 6 months (MD, −6.52 mm; 95% CI, −13.28 to 0.24).

Study details: Findings are from a systematic review and meta-analysis of 33 randomized controlled trials including 2,658 patients with RA.

Disclosures: The study received no specific funding. D McWilliams, DA Walsh, and NG Shanker reported receiving grant support and consultancy fees from various sources like Pfizer Ltd., Eli Lilly, UCB, AbbVie, GSK, and Cambridge Nutraceuticals.

Source: McWilliams DF et al. Rheumatology (Oxford). 2021 Jul 2. doi: 10.1093/rheumatology/keab503.

Key clinical point: Treatment with bazedoxifene for 48 weeks significantly increased bone mineral density (BMD) of L-spine and decreased bone turnover markers in postmenopausal women with rheumatoid arthritis (RA) receiving low-dose glucocorticoids.

Major finding: Treatment with bazedoxifene significantly increased L-spine BMD (0.015 g/cm²; P = .007), whereas the change in the control group was not significant (0.002 g/cm²; P = .694). At 24 weeks, all bone turnover biomarkers decreased significantly with bazedoxifene, which persisted to 48 weeks (all P less than .01), whereas recovery observed in the control group was not significant.

Study details: The data come from an open-label study involving 114 postmenopausal women with osteopenia who had been receiving low-dose glucocorticoids for RA and were randomly assigned to either daily bazedoxifene (20 mg/day) with calcium and vitamin D or only calcium and vitamin D (control group).

Disclosures: The study was supported by a research grant from Pfizer Pharmaceuticals Korea Ltd. YK Sung reported receiving research grants from Bristol-Myers Squibb, Eisai, Pfizer, and JW Pharmaceutical.

Source: Cho SK et al. Arthritis Res Ther. 2021 Jul 2. doi: 10.1186/s13075-021-02564-1.

Key clinical point: Treatment with bazedoxifene for 48 weeks significantly increased bone mineral density (BMD) of L-spine and decreased bone turnover markers in postmenopausal women with rheumatoid arthritis (RA) receiving low-dose glucocorticoids.

Major finding: Treatment with bazedoxifene significantly increased L-spine BMD (0.015 g/cm²; P = .007), whereas the change in the control group was not significant (0.002 g/cm²; P = .694). At 24 weeks, all bone turnover biomarkers decreased significantly with bazedoxifene, which persisted to 48 weeks (all P less than .01), whereas recovery observed in the control group was not significant.

Study details: The data come from an open-label study involving 114 postmenopausal women with osteopenia who had been receiving low-dose glucocorticoids for RA and were randomly assigned to either daily bazedoxifene (20 mg/day) with calcium and vitamin D or only calcium and vitamin D (control group).

Disclosures: The study was supported by a research grant from Pfizer Pharmaceuticals Korea Ltd. YK Sung reported receiving research grants from Bristol-Myers Squibb, Eisai, Pfizer, and JW Pharmaceutical.

Source: Cho SK et al. Arthritis Res Ther. 2021 Jul 2. doi: 10.1186/s13075-021-02564-1.

Key clinical point: Treatment with bazedoxifene for 48 weeks significantly increased bone mineral density (BMD) of L-spine and decreased bone turnover markers in postmenopausal women with rheumatoid arthritis (RA) receiving low-dose glucocorticoids.

Major finding: Treatment with bazedoxifene significantly increased L-spine BMD (0.015 g/cm²; P = .007), whereas the change in the control group was not significant (0.002 g/cm²; P = .694). At 24 weeks, all bone turnover biomarkers decreased significantly with bazedoxifene, which persisted to 48 weeks (all P less than .01), whereas recovery observed in the control group was not significant.

Study details: The data come from an open-label study involving 114 postmenopausal women with osteopenia who had been receiving low-dose glucocorticoids for RA and were randomly assigned to either daily bazedoxifene (20 mg/day) with calcium and vitamin D or only calcium and vitamin D (control group).

Disclosures: The study was supported by a research grant from Pfizer Pharmaceuticals Korea Ltd. YK Sung reported receiving research grants from Bristol-Myers Squibb, Eisai, Pfizer, and JW Pharmaceutical.

Source: Cho SK et al. Arthritis Res Ther. 2021 Jul 2. doi: 10.1186/s13075-021-02564-1.

Key clinical point: In patients with active rheumatoid arthritis (RA), adalimumab biosimilar CT-P17 and reference adalimumab showed comparable efficacy and safety during 1 year of treatment even after switching to CT-P17 from reference adalimumab.

Major finding: At 52 weeks, the proportion of patients achieving a 20%/50%/70% improvement by American College of Rheumatology criteria was comparable among those who continued CT-P17 (80.5%/66.3%/44.6%), continued reference adalimumab (77.8%/62.1%/49.0%), or switched to CT-P17 (82.2%/66.4%/47.4%), respectively. Similar proportions of patients in each treatment group experienced 1 or more treatment-emergent adverse events.

Study details: This was a 52-week, randomized, phase 3 study of 607 patients with active RA who received either 40 mg (100 mg/mL) CT-P17 or reference adalimumab subcutaneously every 2 weeks until week 24. Later, patients receiving CT-P17 continued to receive the same, whereas those receiving reference adalimumab either continued the same or switched to CT-P17.

Disclosures: This work was supported by Celltrion, Inc. Some of the authors reported receiving research grants, consulting, speaker fees, and/or honoraria from various sources. SJ Lee, SH Kim, YJ Bae, GE Yang, and JK Yoo declared being employees of Celltrion, Inc.

Source: Furst DE et al. Rheumatology (Oxford). 2021 Jun 17. doi: 10.1093/rheumatology/keab460.

Key clinical point: In patients with active rheumatoid arthritis (RA), adalimumab biosimilar CT-P17 and reference adalimumab showed comparable efficacy and safety during 1 year of treatment even after switching to CT-P17 from reference adalimumab.

Major finding: At 52 weeks, the proportion of patients achieving a 20%/50%/70% improvement by American College of Rheumatology criteria was comparable among those who continued CT-P17 (80.5%/66.3%/44.6%), continued reference adalimumab (77.8%/62.1%/49.0%), or switched to CT-P17 (82.2%/66.4%/47.4%), respectively. Similar proportions of patients in each treatment group experienced 1 or more treatment-emergent adverse events.

Study details: This was a 52-week, randomized, phase 3 study of 607 patients with active RA who received either 40 mg (100 mg/mL) CT-P17 or reference adalimumab subcutaneously every 2 weeks until week 24. Later, patients receiving CT-P17 continued to receive the same, whereas those receiving reference adalimumab either continued the same or switched to CT-P17.

Disclosures: This work was supported by Celltrion, Inc. Some of the authors reported receiving research grants, consulting, speaker fees, and/or honoraria from various sources. SJ Lee, SH Kim, YJ Bae, GE Yang, and JK Yoo declared being employees of Celltrion, Inc.

Source: Furst DE et al. Rheumatology (Oxford). 2021 Jun 17. doi: 10.1093/rheumatology/keab460.

Key clinical point: In patients with active rheumatoid arthritis (RA), adalimumab biosimilar CT-P17 and reference adalimumab showed comparable efficacy and safety during 1 year of treatment even after switching to CT-P17 from reference adalimumab.

Major finding: At 52 weeks, the proportion of patients achieving a 20%/50%/70% improvement by American College of Rheumatology criteria was comparable among those who continued CT-P17 (80.5%/66.3%/44.6%), continued reference adalimumab (77.8%/62.1%/49.0%), or switched to CT-P17 (82.2%/66.4%/47.4%), respectively. Similar proportions of patients in each treatment group experienced 1 or more treatment-emergent adverse events.

Study details: This was a 52-week, randomized, phase 3 study of 607 patients with active RA who received either 40 mg (100 mg/mL) CT-P17 or reference adalimumab subcutaneously every 2 weeks until week 24. Later, patients receiving CT-P17 continued to receive the same, whereas those receiving reference adalimumab either continued the same or switched to CT-P17.

Disclosures: This work was supported by Celltrion, Inc. Some of the authors reported receiving research grants, consulting, speaker fees, and/or honoraria from various sources. SJ Lee, SH Kim, YJ Bae, GE Yang, and JK Yoo declared being employees of Celltrion, Inc.

Source: Furst DE et al. Rheumatology (Oxford). 2021 Jun 17. doi: 10.1093/rheumatology/keab460.

Recently, ACR guidelines were published on the prevention and treatment of glucocorticoid-induced osteoporosis, emphasizing use of supplemental calcium and vitamin D and antiresorptive therapy. This randomized, controlled, open-label trial by Cho et al looks at the efficacy of selective estrogen receptor modulators (SERMs) in preventing bone loss and fractures in postmenopausal RA patients with osteopenia on long-term glucocorticoids. Patients were randomized to bazedoxefine, a 3^rd-generation SERM vs no therapy in addition to background calcium and vitamin D supplementation and bone mineral density (BMD) and trabecular bone score (TBS). Bone turnover markers were assessed over the course of 48 weeks, in addition to adverse events. Prednisone dose was relatively low, with a baseline of ~3 mg/day. Bone density increased by almost 2% in the L spine (P < 0.05), but the increases in BMD at the femoral neck and TBS were not significant. Bone turnover markers did decrease in the bazedoxefine group, though not in the control group. These findings are not striking but are promising given the short duration of the study (<1 year), and potentially deserves longer-term follow-up, both for evaluation of efficacy as well as long-term safety. In the US, the medication is only available in combination with estrogen, and thus it is not currently a practical option for RA patients with GIOP.

Despite wider availability of both synthetic and biologic DMARDs for treatment of RA in recent years, persistent pain is an issue for many patients, perhaps due to peripheral sensitization. Though it seems almost unnecessary to investigate the utility of glucocorticoids for treatment of RA-related pain, the magnitude and duration of their benefit is unknown. McWilliams et al take the approach of quantitatively analyzing the benefit of glucocorticoids in RA over time in their systematic review and meta-analysis. The study looked at both spontaneous and evoked pain, and evaluated 65 studies that mostly used pain visual analogue scale, tender joint count, and Ritchie Articular Index. Reduction in spontaneous pain was greatest in the 0-3-month time period, with smaller reductions in 3-6 months and >6 month. A similar pattern was seen in evaluation of the time course of evoked pain. As such, the benefits of long-term systemic glucocorticoid therapy may not outweigh its well-known risks, especially in patients with persistent pain. Whether this is due to non-inflammatory sources of pain or other mechanisms remains unknown and is likely heavily impacted by the specific clinical scenario.

Due to the potential long-terms side effects of chronic immunosuppression, including long-term glucocorticoid therapy in patients with persistent pain in RA, the course and predictors of unacceptable pain are of interest. Eberhard et al examined an inception cohort of RA patients in a single center in Sweden over the course of 5 years. They were found to have reduction of VAS pain from inclusion to 6 months, but pain levels largely stayed the same during the rest of the follow-up period. The proportion of patients with unacceptable pain also decreased but remained stable at about 30% after 1 year, with 20% having unacceptable pain and low inflammation and about 10% having high inflammation and unacceptable pain. The study found seropositivity, high inflammatory parameters, high DAS28 and severe patient-reported outcomes to be predictive of high inflammation and unacceptable pain and lower age, higher VAS pain, and low ESR to be predictive of low inflammation and unacceptable pain. These findings highlight the importance of examining non-inflammatory mechanisms of pain as well as identifying treatments; however, in evaluating the risk of immunosuppression and glucocorticoid therapy, it does not guide increasing or reducing treatment in RA patients with persistent pain.

Recently, ACR guidelines were published on the prevention and treatment of glucocorticoid-induced osteoporosis, emphasizing use of supplemental calcium and vitamin D and antiresorptive therapy. This randomized, controlled, open-label trial by Cho et al looks at the efficacy of selective estrogen receptor modulators (SERMs) in preventing bone loss and fractures in postmenopausal RA patients with osteopenia on long-term glucocorticoids. Patients were randomized to bazedoxefine, a 3^rd-generation SERM vs no therapy in addition to background calcium and vitamin D supplementation and bone mineral density (BMD) and trabecular bone score (TBS). Bone turnover markers were assessed over the course of 48 weeks, in addition to adverse events. Prednisone dose was relatively low, with a baseline of ~3 mg/day. Bone density increased by almost 2% in the L spine (P < 0.05), but the increases in BMD at the femoral neck and TBS were not significant. Bone turnover markers did decrease in the bazedoxefine group, though not in the control group. These findings are not striking but are promising given the short duration of the study (<1 year), and potentially deserves longer-term follow-up, both for evaluation of efficacy as well as long-term safety. In the US, the medication is only available in combination with estrogen, and thus it is not currently a practical option for RA patients with GIOP.

Despite wider availability of both synthetic and biologic DMARDs for treatment of RA in recent years, persistent pain is an issue for many patients, perhaps due to peripheral sensitization. Though it seems almost unnecessary to investigate the utility of glucocorticoids for treatment of RA-related pain, the magnitude and duration of their benefit is unknown. McWilliams et al take the approach of quantitatively analyzing the benefit of glucocorticoids in RA over time in their systematic review and meta-analysis. The study looked at both spontaneous and evoked pain, and evaluated 65 studies that mostly used pain visual analogue scale, tender joint count, and Ritchie Articular Index. Reduction in spontaneous pain was greatest in the 0-3-month time period, with smaller reductions in 3-6 months and >6 month. A similar pattern was seen in evaluation of the time course of evoked pain. As such, the benefits of long-term systemic glucocorticoid therapy may not outweigh its well-known risks, especially in patients with persistent pain. Whether this is due to non-inflammatory sources of pain or other mechanisms remains unknown and is likely heavily impacted by the specific clinical scenario.

Due to the potential long-terms side effects of chronic immunosuppression, including long-term glucocorticoid therapy in patients with persistent pain in RA, the course and predictors of unacceptable pain are of interest. Eberhard et al examined an inception cohort of RA patients in a single center in Sweden over the course of 5 years. They were found to have reduction of VAS pain from inclusion to 6 months, but pain levels largely stayed the same during the rest of the follow-up period. The proportion of patients with unacceptable pain also decreased but remained stable at about 30% after 1 year, with 20% having unacceptable pain and low inflammation and about 10% having high inflammation and unacceptable pain. The study found seropositivity, high inflammatory parameters, high DAS28 and severe patient-reported outcomes to be predictive of high inflammation and unacceptable pain and lower age, higher VAS pain, and low ESR to be predictive of low inflammation and unacceptable pain. These findings highlight the importance of examining non-inflammatory mechanisms of pain as well as identifying treatments; however, in evaluating the risk of immunosuppression and glucocorticoid therapy, it does not guide increasing or reducing treatment in RA patients with persistent pain.

Recently, ACR guidelines were published on the prevention and treatment of glucocorticoid-induced osteoporosis, emphasizing use of supplemental calcium and vitamin D and antiresorptive therapy. This randomized, controlled, open-label trial by Cho et al looks at the efficacy of selective estrogen receptor modulators (SERMs) in preventing bone loss and fractures in postmenopausal RA patients with osteopenia on long-term glucocorticoids. Patients were randomized to bazedoxefine, a 3^rd-generation SERM vs no therapy in addition to background calcium and vitamin D supplementation and bone mineral density (BMD) and trabecular bone score (TBS). Bone turnover markers were assessed over the course of 48 weeks, in addition to adverse events. Prednisone dose was relatively low, with a baseline of ~3 mg/day. Bone density increased by almost 2% in the L spine (P < 0.05), but the increases in BMD at the femoral neck and TBS were not significant. Bone turnover markers did decrease in the bazedoxefine group, though not in the control group. These findings are not striking but are promising given the short duration of the study (<1 year), and potentially deserves longer-term follow-up, both for evaluation of efficacy as well as long-term safety. In the US, the medication is only available in combination with estrogen, and thus it is not currently a practical option for RA patients with GIOP.

Despite wider availability of both synthetic and biologic DMARDs for treatment of RA in recent years, persistent pain is an issue for many patients, perhaps due to peripheral sensitization. Though it seems almost unnecessary to investigate the utility of glucocorticoids for treatment of RA-related pain, the magnitude and duration of their benefit is unknown. McWilliams et al take the approach of quantitatively analyzing the benefit of glucocorticoids in RA over time in their systematic review and meta-analysis. The study looked at both spontaneous and evoked pain, and evaluated 65 studies that mostly used pain visual analogue scale, tender joint count, and Ritchie Articular Index. Reduction in spontaneous pain was greatest in the 0-3-month time period, with smaller reductions in 3-6 months and >6 month. A similar pattern was seen in evaluation of the time course of evoked pain. As such, the benefits of long-term systemic glucocorticoid therapy may not outweigh its well-known risks, especially in patients with persistent pain. Whether this is due to non-inflammatory sources of pain or other mechanisms remains unknown and is likely heavily impacted by the specific clinical scenario.

Due to the potential long-terms side effects of chronic immunosuppression, including long-term glucocorticoid therapy in patients with persistent pain in RA, the course and predictors of unacceptable pain are of interest. Eberhard et al examined an inception cohort of RA patients in a single center in Sweden over the course of 5 years. They were found to have reduction of VAS pain from inclusion to 6 months, but pain levels largely stayed the same during the rest of the follow-up period. The proportion of patients with unacceptable pain also decreased but remained stable at about 30% after 1 year, with 20% having unacceptable pain and low inflammation and about 10% having high inflammation and unacceptable pain. The study found seropositivity, high inflammatory parameters, high DAS28 and severe patient-reported outcomes to be predictive of high inflammation and unacceptable pain and lower age, higher VAS pain, and low ESR to be predictive of low inflammation and unacceptable pain. These findings highlight the importance of examining non-inflammatory mechanisms of pain as well as identifying treatments; however, in evaluating the risk of immunosuppression and glucocorticoid therapy, it does not guide increasing or reducing treatment in RA patients with persistent pain.